Review of the literature shows that it is reasonable to propose that, in mammalian muscle resting potential, acetylcholine sensitivity, and the susceptibility of the membrane action potential to inhibition by tetrodotoxin are controlled by a mechanism which works through DNA dependent RNA and protein synthesis and which can be influenced by muscle activity or trophic factors transported down nerve by axoplasmic transport. This working hypothesis will be tested by examining the effect of selective inhibition of muscle activity and axoplasmic transport. The effect of varying the amount of muscle activity and the ability of Actinomycin D to delay the changes caused by selective inhibition of muscle activity and axoplasmic transport will also be examined. The techniques for inhibition of nerve activity and axoplasmic transport developed in this study will be used to investigate the influence of these factors on transmitter release and the structural integrity of the mammalian motorneuron terminal.